期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 280, 期 9, 页码 7519-7529出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M407438200
关键词
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资金
- NHLBI NIH HHS [R01 HL050040, R01 HL050040-10, R01 HL036235-21, HL50040, R01 HL036235, HL36236] Funding Source: Medline
- NIGMS NIH HHS [R01 GM059281, GM59281] Funding Source: Medline
The role of a cytosolic phospholipase A(2)-alpha( cPLA(2)-alpha) in neutrophil arachidonic acid release, platelet-activating factor ( PAF) biosynthesis, NADPH oxidase activation, and bacterial killing in vitro, and the innate immune response to bacterial infection in vivo was examined. cPLA(2)-alpha activity was blocked with the specific cPLA(2)-alpha inhibitor, Pyrrolidine-1 ( human cells), or by cPLA(2)-alpha gene disruption ( mice). cPLA(2)-alpha inhibition or gene disruption led to complete suppression of neutrophil arachidonate release and PAF biosynthesis but had no effect on neutrophil NADPH oxidase activation, FcgammaII/III or CD11b surface expression, primary or secondary granule secretion, or phagocytosis of Escherichia coli in vitro. In contrast, cPLA(2)-alpha inhibition or gene disruption diminished neutrophil-mediated E. coli killing in vitro, which was partially rescued by exogenous arachidonic acid or PAF but not leukotriene B-4. Following intratracheal inoculation with live E. coli in vivo, pulmonary PAF biosynthesis, inflammatory cell infiltration, and clearance of E. coli were attenuated in cPLA(2)-alpha(-I-) mice compared with wild type littermates. These studies identify a novel role for cPLA(2)-alpha in the regulation of neutrophil-mediated bacterial killing and the innate immune response to bacterial infection.
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